Fig 1.
SIRT1 is involved in the attenuation of H2O2-induced senescence by resveratrol.
(a) Human primary keratinocytes (passage 4) showed a number of senescent cells positive for SA-Gal (dark blue-green color). These cells lacked SIRT1 immunostaining (red arrow), which normally appears in the nucleus (see brown color in adjacent cells). (b,c,d) Exposure of human primary keratinocytes to 50 µM H2O2 induced a 5–6 fold increase in SA-Gal expression. The effect of H2O2 was largely prevented by pre-treatment with 50 µM resveratrol for 30 min. Addition of Ex527, a SIRT1-specific inhibitor, prior to the addition of resveratrol did not alter AMPK activation but abrogated the effects of resveratrol on SA-Gal staining. For (d), numbers inside parenthesis denote n. (e) SIRT1 was ectopically expressed by recombinant lentivirus, which produced strong staining within the cytosol (red arrow), instead of nuclear staining in normal cells (gray arrow).
----> I think this may explain why Reservatrol has been labeled at some point as the drug of the future.
The grape or peanuts or black chocolate, etc…
If you read back the papers I have cited here of plos dot org you will understand that they identified anti-aging thus anti-standard-apoptosis effects of resveratrol.